Memantine

Pharmaceuticals -> Synthetic Cannabinoids or Psychoactive Compounds

Pharmaceuticals

log Kow = 3.28

3.5

3.28

soluble in water

4.55e-02 g/L

EMA approved medicines: Human medicine

EMA approved medicines: Human medicine

EMA approved medicines: Human medicine

EMA approved medicines: Human medicine

EMA approved medicines: Human medicine

EMA approved medicines: Human medicine

White to off white fine powder. Crystals from alcohol/ether. MP: 290-295 °C, also reported as 290-295 °C. Soluble in water. /Memantine hydrochloride/

258 °C (hydrochloride salt)

This chemical does not meet GHS hazard criteria for 50% (1 of 2) of reports.

Warning

H302 (50%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 2 reports by companies from 2 notifications to the ECHA C&L Inventory.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including memantine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Memantine hydrochloride/

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

ACCIDENTAL RELEASE MEASURES. Personal precautions, protective equipment and emergency procedures: Avoid dust formation. Avoid breathing vapours, mist or gas.; Environmental precautions: Do not let product enter drains.; Methods and materials for containment and cleaning up: Sweep up and shovel. Keep in suitable, closed containers for disposal.

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Precautions for safe handling: Provide appropriate exhaust ventilation at places where dust is formed.

Respiratory protection: Respiratory protection is not required. Where protection from nuisance levels of dusts are desired, use type N95 (US) or type P1 (EN 143) dust masks. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Body Protection: Choose body protection in relation to its type, to the concentration and amount of dangerous substances, and to the specific work-place., The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Skin protection: Handle with gloves.

Eye/face protection: Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Protein-bound Drugs: Because plasma protein binding of memantine is low (45%), a pharmacokinetic interaction with drugs that are highly protein bound (e.g., digoxin, warfarin) is unlikely.

Drugs Secreted by Renal Tubular Cationic Transport: Potential pharmacokinetic interaction (altered plasma concentrations of both drugs) when memantine is used with drugs secreted by the same renal cationic system (e.g., cimetidine, hydrochlorothiazide, metformin, nicotine, quinidine, ranitidine, triamterene). However, concomitant use of memantine with a fixed combination of hydrochlorothiazide and triamterene did not affect bioavailability of either memantine or triamterene, and maximum plasma concentrations and area under the plasma concentration-time curve (AUC) of hydrochlorothiazide decreased by only 20%. In addition, concomitant use of memantine with a fixed combination of glyburide and metformin hydrochloride did not affect the pharmacokinetics of memantine, metformin, or glyburide, and the hypoglycemic effects of the glyburide-metformin combination were not affected.

Alkalinizing Agents: Potential decreased memantine clearance with resulting increases in adverse effects when drug is used concomitantly with agents that increase urine pH (e.g., carbonic anhydrase inhibitors, sodium bicarbonate). Use with caution. Memantine clearance was decreased by approximately 80% at alkaline urine conditions (ie, pH 8).

Cholinesterase Inhibitors: Concomitant use of memantine with the acetylcholinesterase inhibitor donepezil did not affect the pharmacokinetics of either drug or substantially alter acetylcholinesterase inhibition by donepezil. In a 24-week clinical study in patients with moderate to severe Alzheimer's disease, adverse effects observed with combination therapy with memantine and donepezil were similar to those observed with donepezil alone. In vitro and animal studies indicate that memantine does not affect the reversible inhibition of acetylcholinesterase produced by donepezil, galantamine, or tacrine.

For more Interactions (Complete) data for MEMANTINE (9 total), please visit the HSDB record page.

In large placebo controlled trials, the rate of serum enzyme elevations during memantine therapy was similar to that in patients on placebo and no instances of clinically apparent liver injury were reported. Nevertheless, since its introduction into clinical use, memantine has been implicated in at least one report of clinically apparent hepatotoxicity. The time to onset was 3 weeks and the clinical syndrome was that of an acute cholestatic hepatitis which was mild-to-moderate in severity and rapidly reversible upon drug discontinuation (Case 1). Immunoallergic and autoimmune features were not present.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 660(SRC), determined from a structure estimation method(2), indicates that memantine is expected to have very low mobility in soil(SRC). The estimated pKa of memantine is 10.7(3), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the compound exists as a cation and cations do not volatilize. Memantine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.9X10-4 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2015).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 660(SRC), determined from a structure estimation method(2), indicates that memantine is expected to adsorb to suspended solids and sediment(SRC). An estimated pKa of 10.7(3) indicates memantine will exist almost entirely in the cation form at pH values of 5 to 9 and, therefore, volatilization from water and moist soil surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 70(SRC), from its log Kow of 3.28(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is high(SRC). Biodegradation data in water were not available(SRC, 2015).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), memantine, which has an estimated vapor pressure of 1.9X10-4 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase memantine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 4 hrs(SRC), calculated from its rate constant of 3.3X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Memantine does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

The most common adverse effects of memantine in clinical trials include dizziness, headache, confusion, diarrhea, and constipation. Additional adverse effects include fatigue, pain, hypertension, weight gain, hallucination, confusion, aggressive behavior, vomiting, abdominal pain, and urinary incontinence.

IDENTIFICATION AND USE: Memantine is an oil. It is prescribed as a treatment for moderate to severe Alzheimer's Disease. Memantine functions by blocking the NMDA receptor. HUMAN EXPOSURE AND TOXICITY: Signs and symptoms most often accompanying memantine overdosage in clinical trials and from worldwide marketing experience, alone or in combination with other drugs and/or alcohol, include agitation, asthenia, bradycardia, confusion, coma, dizziness, ECG changes, increased blood pressure, lethargy, loss of consciousness, psychosis, restlessness, slowed movement, somnolence, stupor, unsteady gait, visual hallucinations, vertigo, vomiting, and weakness. Renal impairment and hyperkalaemia possibly associated with memantine administration was described in one patient. Two cases of repeated loss of consciousness were reported after long-term memantine treatment in patients with Alzheimer disease, which resolved after its discontinuation. Little is known about the cardiovascular effects of memantine but there have been reports of bradycardia and reduced cardiovascular survival associated with its use. Memantine produced no evidence of genotoxic potential in vitro in chromosomal aberration test in human lymphocytes. ANIMAL STUDIES: In newborn mice treatment with memantine temporally improves hippocampus-dependent memory formation. In rats memantine administration significantly attenuated the ethanol-associated behavioral alterations in a dose-dependent manner. Memantine produced no evidence of genotoxic potential when evaluated in the in vitro S. typhimurium or E. coli reverse mutation assay, or in vivo cytogenetics assay for chromosome damage in rats, and the in vivo mouse micronucleus assay. The results were equivocal in an in vitro gene mutation assay using Chinese hamster V79 cells.

Memantine overdose can result in several signs and symptoms. These may include agitation, asthenia, confusion, visual hallucinations, vertigo, coma, slowed movement, somnolence, dizziness, lethargy, loss of consciousness, ECG changes, bradycardia, increased blood pressure, psychosis, restlessness, stupor, unsteady gait, vomiting, and weakness. Clinicians must be aware of these potential effects when using memantine alone or in combination with other drugs and/or alcohol.

Memantine exerts its action through uncompetitive NMDA receptor antagonism, binding preferentially to the NMDA receptor-operated cation channels. Prolonged increased levels of glutamate in the brain of demented patients are sufficient to counter the voltage-dependent block of NMDA receptors by Mg²⁺ ions and allow continuous influx of Ca²⁺ ions into cells, ultimately resulting in neuronal degeneration. Studies suggest that memantine binds more effectively than Mg²⁺ ions at the NMDA receptor, and thereby effectively blocks this prolonged influx of Ca²⁺ ions through the NMDA channel whilst preserving the transient physiological activation of the channels by higher concentrations of synaptically released glutamate. Thus memantine protects against chronically elevated concentrations of glutamate. Memantine also has antagonistic activity at the type 3 serotonergic (5-HT₃) receptor with a potency that is similar to that at the NMDA receptor, and lower antagonistic activity at the nicotinic acetylcholine receptor. This drug has no affinity for gamma-aminobutyric acid (GABA), benzodiazepine, dopamine, adrenergic, histamine, or glycine receptors or for voltage-dependent calcium, sodium, or potassium channels.

Side effects include pain, abnormal crying, leg pain, fever, increased apetite. Adverse drug reactions include: dizziness, confusion, headache, hallucinations, tiredness. Less common side effects include: vomiting, anxiety, hypertonia, cystitis, and increased libido. Doses of up to 400 mg have been tolerated.

Memantine was present in 88% of effluent samples from 90 European wastewater treatment plants at an average concentration of 22.8 ng/L; median concentration 3.7 ng/L, maximum concentration 1312 ng/L, limit of quantitation 0.5 ng/L. The samples were from plants in Austria, Belgium, Czech Republic, Cyprus, Finland, France, Germany, Greece, Hungary, Ireland, Italy, Lithuania, Netherlands, Portugal, Slovenia, Spain, Sweden and Switzerland. Sampling was conducted in 2010(1).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of memantine can be estimated to be 660(SRC). According to a classification scheme(2), this estimated Koc value suggests that memantine is expected to have low mobility in soil. The estimated pKa of memantine is 10.7(3), indicating that this compound will exist almost entirely in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

/HUMAN EXPOSURE STUDIES/ The authors retrospectively reviewed the clinical records of 196 patients with dementia treated with memantine for at least 6 months. Eleven (5.6%) developed treatment-induced agitation. At chi-square analysis, they were significantly more likely to have a history of similar side effects from other medications acting on the central nervous system in comparison with the group without agitation, suggesting neurochemical susceptibility. A trend toward a significantly greater prevalence was also present for ischemic cardiopathy and neuroimaging evidence of chronic small vessel disease. Ischemic brain and heart disease might contribute through anatomical and functional alterations within the glutamatergic system.

/HUMAN EXPOSURE STUDIES/ Abstract AIM: Memantine hydrochloride (Memary), launched in June 2011 in Japan, is used in patients with moderate to severe Alzheimer's disease. We performed an integrated analysis of data obtained from different clinical studies of memantine hydrochloride conducted between 2002 and 2011 in Japan in order to examine the long-term tolerability and efficacy of this drug at a dose of 20 mg/day. METHODS: Using clinical studies of memantine hydrochloride performed in Japan between 2002 and 2011, the therapeutic safety and the time course of MMSE scores in 702 subjects who had received memantine hydrochloride were examined. RESULTS: The mean duration of memantine treatment was 798.1 days, with the longest duration of 3,373 days (approximately nine years and two months). The incidence of adverse events every 52 weeks of treatment ranged from 71.0% to 88.9%, and the incidence of adverse drug reactions ranged from 5.6% to 32.1%, with no associations between the incidence of adverse events and the treatment duration. There were no adverse drug reactions specific to the long-term administration of this drug. The occurrence of "adverse events" was the primary reason for drug discontinuation. During the long-term study observation period, there were many cases of adverse events and treatment discontinuation due to the background factors of the subjects, including adverse events associated with aging and progression of the underlying conditions. In addition, treatment discontinuation was also associated with admission to a nursing home or facility due to changes in home nursing care. The degree of MMSE score reduction over time was lower in the patients treated with memantine than the expected MMSE score reduction observed in the untreated patients. CONCLUSIONS: Based on these findings, there are no issues regarding the tolerability of memantine hydrochloride administered at a dose of 20 mg/day over the long term. Considering changes in the MMSE score, the results indicated that memantine hydrochloride may inhibit worsening of the cognitive function for long periods of time in patients with Alzheimer's disease.

/HUMAN EXPOSURE STUDIES/ Abstract OBJECTIVE: Enhanced N-methyl-D-aspartate (NMDA) receptor function associated with a positive family history of alcoholism (FHP) has been hypothesized to contribute to the heritable risk for alcoholism. The objective of this study was to evaluate the relationship of alcoholism family history, NMDA receptor function, and cortical information processing by testing acute effects of the NMDA receptor antagonist memantine on event-related potential (ERP). METHOD: Twenty-two healthy FHP and 20 healthy family history-negative (FHN; no alcoholic relatives) subjects were administered placebo or 40 mg of memantine under double-blind counterbalanced conditions on two separate occasions. Electroencephalogram data were collected from eight channels with eyes open during an auditory oddball discrimination task. We evaluated P3b amplitude, total theta, alpha activity, and fractal dimension from ERP trials. RESULTS: FHP and FHN subjects did not differ in P3b amplitude. A significant Group x Drug interaction was observed in theta, alpha activity, and fractal dimension at the parietal and occipital sites. FHP individuals exhibited significantly higher fractal dimension and lower theta and alpha activity after placebo relative to FHN subjects. Following memantine administration, theta activity decreased in both groups but more markedly for FHN individuals. Alpha activity decreased for FHN subjects and increased for FHP individuals, whereas the fractal dimension decreased for FHP subjects and increased for FHN subjects after memantine. CONCLUSIONS: A plausible interpretation of these results is that FHP individuals may have altered NMDA receptor function compared with FHN individuals. These findings provide additional evidence of differences in the regulation of NMDA receptor function between FHP and FHN individuals.

/SIGNS AND SYMPTOMS/ Signs and symptoms most often accompanying memantine overdosage in clinical trials and from worldwide marketing experience, alone or in combination with other drugs and/or alcohol, include agitation, asthenia, bradycardia, confusion, coma, dizziness, ECG changes, increased blood pressure, lethargy, loss of consciousness, psychosis, restlessness, slowed movement, somnolence, stupor, unsteady gait, visual hallucinations, vertigo, vomiting, and weakness.

For more Human Toxicity Excerpts (Complete) data for MEMANTINE (8 total), please visit the HSDB record page.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including memantine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Memantine hydrochloride/

N06DX01

N - Nervous system

QN - Nervous system

**General effects** This drug inhibits calcium influx into cells that is normally caused by chronic NMDA receptor activation by glutamate. This leads to the improvement of Alzheimer's dementia symptoms, demonstrated by increased cognition and other beneficial central nervous system effects. **Effects on neuroplasticity** Like other NMDA receptor antagonists, memantine at high doses can reduce neuronal synaptic plasticity that is involved in learning and memory processes. At lower concentrations, which are normally used in the clinical setting, memantine can enhance neuronal synaptic plasticity in the brain, improve memory, and act as a neuroprotectant against the destruction of neurons caused by excitatory neurotransmitters. **Effect on various receptors** Memantine has demonstrated minimal activity for GABA, benzodiazepine, dopamine, adrenergic, histamine, and glycine receptors, as well as voltage-dependent Ca2+, Na+ or K+ channels. This drug has shown antagonist activity at the 5HT3 receptors. Laboratory studies suggest that memantine does not affect the reversible inhibition of the acetylcholinesterase normally caused by donepezil, galantamine, or tacrine.

Continuous activation of the N-methyl-D-aspartate (NMDA) receptors in the central nervous system caused by _glutamate_ is thought to cause some of the Alzheimer's disease symptoms. This overactivation is thought to contribute to neurotoxicity due to the excitatory properties of glutamate. The pharmacological effect of memantine likely occurs via the drug's behavior as an uncompetitive (open-channel) NMDA receptor antagonist, preventing glutamate action on this receptor. Memantine has a preference for the NMDA receptor-operated cation channels. Despite these antagonist effects, memantine has not been proven to prevent or retard the neurodegeneration seen in patients diagnosed with Alzheimer’s disease.

In addition to exhibiting antagonists activity at the NMDA receptor, memantine exhibits antagonist activity at the type 3 serotonergic (5-HT3) receptor with a potency that appears to be similar to that at the NMDA receptor. Memantine also blocks the nicotinic acetylcholine receptor with a potency of about one-sixth to one-tenth that at the NMDA receptor. Memantine exhibits little or no affinity for gamma-aminobutyric acid (GABA), benzodiazepine, dopamine, adrenergic, histamine, or glycine receptors or for voltage-dependent calcium, sodium, or potassium channels.

Memantine is a similar uncompetitive NMDA-receptor antagonist to MK-801 and phencyclidine (PCP), and it prevents nerve cell death induced by the ischemia which induces as excessive release of glutamate. These medicines act on an ion channel binding site similar to the magnesium ion binding site. However, MK-801 and PCP cause schizophrenic symptoms, so they are not being used as a therapeutic drug for Alzheimer's Disease. Memantine does not have those toxicities and does not stimulate acetylcholine release in the cerebral cortex. Although the mechanism of the difference from memantine and MK-801 has not been made clear yet, it seems that memantine is combined and released with the ion channel depending on electric potential in the same way as the magnesium ion.

As an uncompetitive inhibitor of the NMDA receptor, memantine, as with MK-801, does not block the binding of the neurotransmitter ,glutamate, to the receptor but rather blocks the ion current through the receptor channel that is activated by glutamate. ... Unlike such high affinity antagonist (MK-80), memantine blocks the NMDA receptor with relatively strong voltage dependence and rapid blocking/unblocking kinetics, dissociating from the NMDA receptors in response to membrane depolarization more readily than MK-801. ... Memantine is able to dissociate from the receptor in response to the strong, transient depolarizations that trigger physiological NMDA receptor activity, while blocking the receptor channels during the chronic, low level excitation that is thought to occur in neurodegenerative diseases such as Alzheimer's disease.

Memantine (Namenda) is prescribed as a treatment for moderate to severe Alzheimer's Disease. Memantine functions by blocking the NMDA receptor, but the key binding interactions between drug and receptor are not fully elucidated. To determine key binding interactions of memantine, we made side-by-side comparisons of IC(50) for memantine and amantadine, a structurally related drug, in the GluN1/GluN2B NMDA receptor. We identified hydrophobic binding pockets for the two methyl groups on memantine formed by the residues A645 and A644 on the third transmembrane helices of GluN1 and GluN2B, respectively. Moreover, we found that while adding two methyl groups to amantadine to produce memantine greatly improves affinity, adding a third methyl group to produce the symmetrical trimethylamantadine diminished affinity. Our results provide a better understanding of chemical-scale interactions between memantine and the NMDA channel, which will potentially benefit the development of new drugs for neurodegenerative diseases involving NMDA receptors.

The terminal elimination half-life of memantine ranges from 60 to 80 hours in humans. Following administration of a single oral dose of 10 mg/kg memantine in rats, the elimination half-life was 2.36 ± 0.20 hours. Following a single intravenous dose of 2 mg/kg in rats, the elimination half-life was 2.28 ± 0.48 hours.

The terminal elimination half-life of memantine is approximately 60-80 hours.

This drug is partially metabolized in the liver. The hepatic CYP450 enzyme system does not majorly contribute to the metabolism of this drug.

Memantine undergoes partial hepatic metabolism. The hepatic microsomal CYP450 enzyme system does not play a significant role in the metabolism of memantine.

The hepatic microsomal cytochrome P-450 (CYP) isoenzyme system does not play a substantial role in the metabolism of memantine.

Excreted largely unchanged. About 20% is metabolized to 1-amino-3-hydroxymethyl-5-methyl-adamantane and 3-amino-1-hydroxy-5,7-dimethyl-adamantane. Route of Elimination: Memantine undergoes partial hepatic metabolism. About 48% of administered drug is excreted unchanged in urine; the remainder is converted primarily to three polar metabolites which possess minimal NMDA receptor antagonistic activity: the N-glucuronide conjugate, 6-hydroxy memantine, and 1-nitroso-deaminated memantine. It is excreted predominantly in the urine, unchanged. Half Life: 60-100 hours

W8O17SJF3T

MEMANTINE

Mechanisms of Action [MoA] - NMDA Receptor Antagonists

Established Pharmacologic Class [EPC] - N-methyl-D-aspartate Receptor Antagonist

Memantine is a N-methyl-D-aspartate Receptor Antagonist. The mechanism of action of memantine is as a NMDA Receptor Antagonist.

MEMANTINE

Agents used in the treatment of Parkinson's disease. The most commonly used drugs act on the dopaminergic system in the striatum and basal ganglia or are centrally acting muscarinic antagonists.

Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.

Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.

After an oral dose, memantine is well absorbed. Its peak drug concentrations are attained in about 3-7 hours. Memantine shows linear pharmacokinetics when given at normal therapeutic doses. This drug can be taken without regard to food, as there is no effect of food on memantine absorption.

This drug is mainly excreted in the urine. Approximately 48% of administered memantine is excreted unchanged in urine. The remainder of the drug is metabolized to three main metabolites. These metabolites are the N-glucuronide conjugate, 6-hydroxy memantine, and 1-nitroso-deaminated memantine, which show minimal NMDA receptor antagonist activity.

The mean volume of distribution of memantine is 9-11 L/kg.

This drug is cleared by active tubular secretion in the kidneys. Tubular reabsorption of this drug is pH dependent.

Memantine is excreted predominantly (about 48%) unchanged in urine and has a terminal elimination half-life of about 60-80 hours. The remainder is converted primarily to three polar metabolites which possess minimal NMDA receptor antagonistic activity: the N-glucuronide conjugate, 6-hydroxy memantine, and 1-nitroso-deaminated memantine. A total of 74% of the administered dose is excreted as the sum of the parent drug and the N-glucuronide conjugate. Renal clearance involves active tubular secretion moderated by pH dependent tubular reabsorption.

Following oral administration memantine is highly absorbed with peak concentrations reached in about 3-7 hours. Memantine has linear pharmacokinetics over the therapeutic dose range. Food has no effect on the absorption of memantine.

MEDICATION

MEDICATION (VET)

Antiparkinson Agents; Dopamine Agents; Excitatory Amino Acid Antagonists

Use (kg; approx.) in Germany (2009): >500

For the treatment of moderate to severe dementia of the Alzheimer's type.

NMDA-receptor antagonist; derivative of adamantane.

Information available in 2005 indicated that Memantine hydrochloride was used in the manufacture of pharmaceutical preparations in the following countries: Argentina, Australia, Austria, Belgium, Colombia, Denmark, Dominican Republic, El Salvador, Finland, France, Germany, Guatemala, Honduras, Hungary, Ireland, Luxembourg, Norway, Panama, Russian Federation, Spain, Switzerland, United Kingdom, United States (1,2)